[1]赵瑞琛 李建国.线粒体质量控制在心肾综合征中的研究进展[J].心血管病学进展,2026,(2):12.[doi:10.16806/j.cnki.issn.1004-3934.2026.02.012]
　ZHAO Ruichen LI Jianguo.Mitochondrial Quality Control in Cardiorenal Syndrome[J].Advances in Cardiovascular Diseases,2026,(2):12.[doi:10.16806/j.cnki.issn.1004-3934.2026.02.012]
点击复制

线粒体质量控制在心肾综合征中的研究进展()

《心血管病学进展》[ISSN:51-1187/R/CN:1004-3934]

卷:
期数:
2026年2期
页码:
12
栏目:
综述
出版日期:
2026-02-25

文章信息/Info

Title:
Mitochondrial Quality Control in Cardiorenal Syndrome
作者:
赵瑞琛1; 2 李建国1; 2
(1.山西医科大学研究生学院,山西 太原 030001;2.山西省汾阳医院(山西医药学院附属第一医院)
Author(s):
ZHAO Ruichen1; 2 LI Jianguo1; 2
(1.Graduate School of Shanxi Medical University,Taiyuan 030001,Shanxi,China;2. Fenyang Hospital of Shanxi Province(The First Affiliated Hospital of Shanxi University of Medicine),Fenyang 032200, Shanxi,China)
关键词:
心肾综合征; 线粒体质量控制; 线粒体生物合成; 线粒体动力学; 线粒体自噬
Keywords:
Cardiorenal syndrome; Mitochondrial quality control; Mitochondrial biogenesis; Mitochondrial dynamics; Mitophagy
DOI:
10.16806/j.cnki.issn.1004-3934.2026.02.012
摘要:
心肾综合征（CRS）以心脏和肾脏功能双向损伤为特征，单一脏器原发损伤可引发另一脏器继发损伤。线粒体作为细胞能量代谢的核心细胞器，其质量控制对维持细胞稳态至关重要。多项研究证明线粒体质量控制（MQC）在心肾疾病中居核心地位，维持线粒体稳态可能成为有前景的治疗策略。本文综述MQC在CRS中的作用与最新进展，并评估其作为治疗靶点的可行性及前景，为CRS的机制研究与诊治提供参考。 【
Abstract:
Cardiorenal syndrome (CRS) is characterized by bidirectional dysfunction of the heart and kidney, wherein primary injury in one organ may lead to secondary injury in the other. Mitochondria, as central organelles governing cellular energy metabolism, play a critical role in maintaining cellular homeostasis, and their quality control is essential. Accumulating evidence indicates that mitochondrial quality control (MQC) occupies a central position in heart and kidney diseases involved in CRS. Maintaining mitochondrial homeostasis may thus represent a promising therapeutic strategy. This review summarizes recent advances in the understanding of MQC in CRS and evaluates its feasibility and prospects as a therapeutic target, thereby providing insights for mechanistic research and clinical management of CRS

参考文献/References:

[1] Rangaswami J,Bhalla V,Blair JEA,et al. Cardiorenal syndrome:classification,pathophysiology,diagnosis,and treatment strategies:a scientific statement from the american heart association[J]. Circulation,2019,139(16):e840-e878.

[2] Adams RA,Liu Z,Hsieh C,et al. Structural analysis of mitochondria in cardiomyocytes:insights into bioenergetics and membrane remodeling[J]. Curr Issues Mol Biol,2023,45(7):6097-6115.

[3] Pagliarini DJ,Calvo SE,Chang B,et al. A mitochondrial protein compendium elucidates complex I disease biology[J]. Cell,2008,134(1):112-123.

[4] Liu TT,Sun WB,Guo SH,et al. Role of mitochondrial quality control in neurodegenerative disease progression[J]. Front Cell Neurosci,2025,19:1588645.

[5] Qian L,Zhu YL,Deng C,et al. Peroxisome proliferator-activated receptor gamma coactivator-1 (PGC-1) family in physiological and pathophysiological process and diseases[J]. Signal Transduct Target Ther,2024,9(1):50.

[6] Chen W,Zhao HK,Li YS. Mitochondrial dynamics in health and disease:mechanisms and potential targets[J]. Signal Transduct Target Ther,2023,8(1):333.

[7] Lu YY,Li ZJ,Zhang SQ,et al. Cellular mitophagy:mechanism, roles in diseases and small molecule pharmacological regulation[J]. Theranostics,2023,13(2):736-766.

[8] Liu BH,Xu CZ,Liu Y,et al. Mitochondrial quality control in human health and disease[J]. Mil Med Res,2024,11(1):32.

[9] Liu L,Li YJ,Wang JN,et al. Mitophagy receptor FUNDC1 is regulated by PGC-1α/NRF1 to fine tune mitochondrial homeostasis[J]. EMBO Rep,2021,22(3):e50629.

[10] Peng KG,Xiao JS,Yang LK,et al. Mutual antagonism of PINK1/Parkin and PGC-1α contributes to maintenance of mitochondrial homeostasis in rotenone-induced neurotoxicity[J]. Neurotox Res,2019,35(2):331-343.

[11] Cheng YH,Huang PX,Zou QX,et al. Nicotinamide mononucleotide alleviates seizures via modulating SIRT1-PGC-1α mediated mitochondrial fusion and fission[J]. J Neurochem,2024,168(12):3962-3981.

[12] Feng R,Liu JY,Yao TT,et al. Neurotoxicity of realgar:crosstalk between UBXD8-Drp1-regulated mitochondrial fission and PINK1-parkin-mediated mitophagy[J]. Mol Neurobiol,2025,62(6):7041-7053.

[13] Du LX,Lu HL,Wang ZY,et al. Therapeutic potential of ginsenoside Rb1-PLGA nanoparticles for heart failure treatment via the ROS/PPARα/PGC1α pathway[J]. Molecules,2023,28(24):8118.

[14] Zhou Z,Song Z,Guo X,et al. Ginsenoside Rb1 ameliorates heart failure ventricular remodeling by regulating the Twist1/PGC-1 α/PPARα signaling pathway[J]. Pharmaceuticals(Basel),2025,18(4):500.

[15] Lyu YT,Huo JY,Jiang WY,et al. Empagliflozin ameliorates cardiac dysfunction in heart failure mice via regulating mitochondrial dynamics[J]. Eur J Pharmacol,2023,942:175531.

[16] Su HX,Xu LL,Li PB,et al. Psmb8 inhibits mitochondrial fission and alleviates myocardial ischaemia/reperfusion injury by targeting Drp1 degradation[J]. Cell Death Dis,2024,15(11):803.

[17] Nàger M,Larsen KB,Bhujabal Z,et al. Mitophagy is induced in human engineered heart tissue after simulated ischemia and reperfusion[J]. J Cell Sci,2025,138(9):jcs263408.

[18] Ai L,de Freitas Germano J,Huang C,et al. Enhanced parkin-mediated mitophagy mitigates adverse left ventricular remodelling after myocardial infarction:role of pr-364[J]. Eur Heart J,2025,46(4):380-393.

[19] Li Q,Liu Y,Huang Q,et al. Hypoxia acclimation protects against heart failure postacute myocardial infarction via FUNDC1-mediated mitophagy[J]. Oxid Med Cell Longev,2022,2022:8192552.

[20] Chen S,Zhang M,Li J,et al. β-catenin-controlled tubular cell-derived exosomes play a key role in fibroblast activation via the OPN-CD44 axis[J]. J Extracell Vesicles,2022,11(3):e12203.

[21] Huang J,Meng P,Liang Y,et al. Tubular CD44 plays a key role in aggravating AKI through NF-κB p65-mediated mitochondrial dysfunction[J]. Cell Death Dis,2025,16(1):119.

[22] Xie HY,Yang NH,Lu L,et al. Uremic toxin receptor AhR facilitates renal senescence and fibrosis via suppressing mitochondrial biogenesis[J]. Adv Sci,2024,11(33):e2402066.

[23] Song ZX,Xia Y,Shi L,et al. Inhibition of Drp1-Fis1 interaction alleviates aberrant mitochondrial fragmentation and acute kidney injury[J]. Cell Mol Biol Lett,2024,29(1):31.

[24] Zhang SQ,Qian SB,Liu HL,et al. LRRK2 aggravates kidney injury through promoting MFN2 degradation and abnormal mitochondrial integrity[J]. Redox Biol,2023,66:102860.

[25] Sun L,Yuan Q,Xu TH,et al. Pioglitazone improves mitochondrial function in the remnant kidney and protects against renal fibrosis in 5/6 nephrectomized rats[J]. Front Pharmacol,2017,8:545.

[26] Zhu XY,Lin QS,Yang YT,et al. Αklotho modulates BNIP3-mediated mitophagy by regulating Foxo3 to decrease mitochondrial ROS and apoptosis in contrast-induced acute kidney injury[J]. Cell Mol Life Sci,2024,81(1):454.

[27] Zhang M,Liu M,Wang T,et al. LncRNA H19 overexpression protects against acute kidney injury after cardiopulmonary bypass via activating Pink1/Parkin-mediated mitophagy[J]. Chin Med J(Engl),2025. DOI:10.1097/CM9.0000000000003552.

[28] Zhang YM,Liu YQ,Bi X,et al. NLRP3 deletion attenuated angiotensin II-induced renal fibrosis by improving mitochondrial dysfunction and endoplasmic reticulum stress[J]. Nephron,2021,145(5):518-527.

[29] Fuhrmann DC,Brüne B. Mitochondrial composition and function under the control of hypoxia[J]. Redox Biol,2017,12:208-215.

[30] Huang YH,Wang SB,Zhou J,et al. IRF1-mediated downregulation of PGC1α contributes to cardiorenal syndrome type 4[J]. Nat Commun,2020,11(1):4664.

[31] Zhao L,Tian L,Wang SW,et al. Levosimendan in rats decreases acute kidney injury after cardiopulmonary resuscitation by improving mitochondrial dysfunction[J]. Transl Androl Urol,2021,10(7):3010-3020.

[32] Yang CC,Yue Y,Chen YL,et al. Febuxostat therapy improved the outcomes of cardiorenal syndrome rodent through alleviating xanthine oxidase-induced oxidative stress and mitochondrial dysfunction[J]. Int J Biol Sci,2025,21(4):1749-1766.

[33] Yang CC,Chen KH,Yue Y,et al. SGLT2 inhibitor downregulated oxidative stress via activating AMPK pathway for cardiorenal (CR) protection in CR syndrome rodent fed with high protein diet[J]. J Mol Histol,2024,55(5):803-823.

[34] Neres-Santos RS,Junho CVC,Panico K,et al. Mitochondrial dysfunction in cardiorenal syndrome 3:renocardiac effect of vitamin C[J]. Cells,2021,10(11):3029.

[35] Liu NY,Ding YQ,Zhou H,et al. Dual-specificity phosphatase 1 interacts with prohibitin 2 to improve mitochondrial quality control against type-3 cardiorenal syndrome[J]. Int J Med Sci,2024,21(3):547-561.

[36] Sumida M,Doi K,Ogasawara E,et al. Regulation of mitochondrial dynamics by dynamin-related protein-1 in acute cardiorenal syndrome[J]. J Am Soc Nephrol,2015,26(10):2378-2387.

[37] Wang J,Wang X,Du W,et al. BI-1 ameliorates myocardial injury by activating the mitochondrial unfolded protein response and FUNDC1-related mitophagy in cardiorenal syndrome type 3[J]. Cell Signal,2022,91:110218.

[38] Bigelman E,Cohen L,Aharon-Hananel G,et al. Pathological presentation of cardiac mitochondria in a rat model for chronic kidney disease[J]. PLoS ONE,2018,13(6):e0198196.

[39] Chen YX,Wei C,Bin L,et al. The potential role of hydrogen sulfide in regulating macrophage phenotypic changes via PINK1/Parkin-mediated mitophagy in sepsis-related cardiorenal syndrome[J]. Immunopharmacol Immunotoxicol,2024,46(2):139-151.

[40] Cai C,Wu F,Zhuang BJ,et al. Empagliflozin activates Wnt/β-catenin to stimulate FUNDC1-dependent mitochondrial quality surveillance against type-3 cardiorenal syndrome[J]. Mol Metab,2022,64:101553.

[41] Shen Y,Peng XJ,Ji HZ,et al. Dapagliflozin protects heart function against type-4 cardiorenal syndrome through activation of PKM2/PP1/FUNDC1-dependent mitophagy[J]. Int J Biol Macromol,2023,250:126116.

[42] Dong X,Wen RJ,Xiong YY,et al. Emodin alleviates CRS4-induced mitochondrial damage via activation of the PGC1α signaling[J]. Phytother Res,2024,38(3):1345-1357.

[43] Ishikita A,Matoba T,Ikeda G,et al. Nanoparticle-mediated delivery of mitochondrial division inhibitor 1 to the myocardium protects the heart from ischemia-reperfusion injury through inhibition of mitochondria outer membrane permeabilization:a new therapeutic modality for acute myocardial infarction[J]. J Am Heart Assoc,2016,5(7):e003872.

[44] Zhang JX,Gu LW,Jiang YM,et al. Artesunate-nanoliposome-TPP,a novel drug delivery system that targets the mitochondria, attenuates cisplatin-induced acute kidney injury by suppressing oxidative stress and inflammatory effects[J]. Int J Nanomedicine,2024,19:1385-1408.

[45] Li Y,Li XM,Wei LS,et al. Advancements in mitochondrial-targeted nanotherapeutics:overcoming biological obstacles and optimizing drug delivery[J]. Front Immunol,2024,15:1451989.

相似文献/References:

[1]金亮丽 王治.现代医学影像学在心肾综合征中的应用进展[J].心血管病学进展,2021,(7):645.[doi:10.16806/j.cnki.issn.1004-3934.2021.07.017]
　JIN Liangli,WANG Zhi.Application Progress of Modern Medical Imaging Technology in Cardiorenal Syndrome[J].Advances in Cardiovascular Diseases,2021,(2):645.[doi:10.16806/j.cnki.issn.1004-3934.2021.07.017]
[2]张国贤 彭瑜 张钲.冠状动脉内皮细胞线粒体损伤在心肌梗死中的研究进展[J].心血管病学进展,2023,(3):203.[doi:10.16806/j.cnki.issn.1004-3934.2023.03.003]
　ZHANG Guoxian,PENG Yu,ZHANG Zheng.Mitochondrial Injury of Coronary Endothelial Cells in Myocardial Infarction[J].Advances in Cardiovascular Diseases,2023,(2):203.[doi:10.16806/j.cnki.issn.1004-3934.2023.03.003]
[3]薛超 吴弘.脑利尿钠肽及N末端脑钠肽前体在心肾综合征患者中的应用进展[J].心血管病学进展,2023,(6):546.[doi:10.16806/j.cnki.issn.1004-3934.2023.06.015]
　XUE Chao,WU Hong.Brain Natriuretic Peptide and N-Terminal Pro-Brain Natriuretic Peptide Application in Cardiorenal Syndrome[J].Advances in Cardiovascular Diseases,2023,(2):546.[doi:10.16806/j.cnki.issn.1004-3934.2023.06.015]
[4]张严 宋可欣 姚朱华.钠-葡萄糖共转运蛋白2抑制剂对心肾综合征获益机制的研究进展[J].心血管病学进展,2024,(5):389.[doi:10.16806/j.cnki.issn.1004-3934.2023.05.002]
　ZHANG Yan,SONG Kexin,YAO Zhuhua.Advances in the Beneficial Mechanisms of Sodium-Glucose Co-Transporter 2 Inhibitor in Cardiorenal Syndrome[J].Advances in Cardiovascular Diseases,2024,(2):389.[doi:10.16806/j.cnki.issn.1004-3934.2023.05.002]
[5]王心雨 王钰淇 罗皓文 常盼 赵晓红.线粒体质量控制在阿霉素诱导的心脏毒性中的研究进展[J].心血管病学进展,2025,(4):318.[doi:10.16806/j.cnki.issn.1004-3934.2025.04.008]
　WANG Xinyu,WANG Yuqi,LUO Haowen,et al.Research Progress of Mitochondrial Quality Control in Doxorubicin Cardiotoxicity[J].Advances in Cardiovascular Diseases,2025,(2):318.[doi:10.16806/j.cnki.issn.1004-3934.2025.04.008]
[6]杨春睿 杨欢 董珊珊 李婷 白彝华 何振坤.Ⅳ型心肾综合征发病机制研究进展[J].心血管病学进展,2025,(10):902.[doi:10.16806/j.cnki.issn.1004-3934.2025.10.009]
　YANG Chunrui,YANG Huan,DONG Shanshan,et al.Pathogenesis of Type Cardiorenal Syndrome[J].Advances in Cardiovascular Diseases,2025,(2):902.[doi:10.16806/j.cnki.issn.1004-3934.2025.10.009]
[7]白慧茹 庞建中.心血管-肾脏-代谢综合征的提出与临床现状[J].心血管病学进展,2025,(12):1071.[doi:10.16806/j.cnki.issn.1004-3934.2025.12.004]
　BAI Huiru,PANG Jianzhong.Proposal and Clinical Status of Cardiovascular-Kidney-Metabolic Syndrome[J].Advances in Cardiovascular Diseases,2025,(2):1071.[doi:10.16806/j.cnki.issn.1004-3934.2025.12.004]

更新日期/Last Update: 2026-05-28